Interlaminar astroglial processes in the cerebral cortex of non human primates: response to injury.
At variance with the rodent, presence of long glial fibrillary acid protein-immunoreactive (GFAP-IR) astroglial processes traversing several cortical laminae (interlaminar processes) appears to be characteristic of the primate cerebral cortex. Their permanence or changes may constitute a significant factor in the functional alterations that develop after brain injury. The immediate and long term response of such astroglial processes to local application of KCl or lesioning, respectively, was analyzed in the striate cortex of adult Cebus apella monkeys. Intraparenchymal injection of 5 mM (within physiological range) or 50 mM (injury levels) KCl into the striate cortex of Cebus apella monkeys resulted three hours later in increased GFAP immunoreactivity in astroglial cells and processes, in the development of numerous foldings and thickenings of GFAP-IR filaments, as compared to mechanical lesioning alone. Such changes were not observed in a cortical region that approximately included laminae IV and V. These results suggest that the immediate GFAP-IR response to KCl cannot be solely explained on the basis of an exposure of new GFAP epitopes due to conformational changes following K-induced cell oedema, or to disaggregation of such filaments. Three months after mechanical lesioning of the frontal and striate cortex, interlaminar processes were absent up to 1.0 mm from the lesion site, and a predominant astrocytosis was present. Long term effects of mechanical lesioning on interlaminar processes resulted in a persistent reduction of these long processes in the vicinity of the lesion, suggesting a significant and prolonged alteration of the astroglial architecture in the adult primate cerebral cortex. It is speculated that these astroglial changes may bear a relationship with the functional alterations observed during the recovery process after brain injury.
Colombo
J A
JA
Programa Unidad de Neurobiología Aplicada (PRUNA) (CEMIC-CONICET), Buenos Aires, Argentina. colombo@pruna.gov.ar
Yáñez
A
A
Lipina
S J
SJ
D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000502:physiology*; D001930:Brain Injuries / Q000378:metabolism / Q000473:pathology*; D002428:Cebus; D002540:Cerebral Cortex / Q000293:injuries* / Q000378:metabolism / Q000473:pathology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology; D014793:Visual Cortex / Q000378:metabolism / Q000473:pathology
D005904:Glial Fibrillary Acidic Protein; D011188:Potassium